37 RAS Flashcards

1
Q

Endogenous peptides play an important role in normal cardiovascular and fluid homeostasis. What do they interact with?

A
  1. Effector organs
  2. Peripheral nervous system
  3. CNS via circumventricular organs
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2
Q

What are the 3 CVOs?

A

Area postrema
subfornical organ
organum vasculosum of the lamina terminalis

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3
Q

What converts angiotensinogen to angiotensin I? angiotensin I to angiotensin II? and on to III?

A

Renin
ACE
Aminopeptidases

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4
Q

What receptors does angiotensin I and II act on? III?

A

At2R and AT1R

AT1R

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5
Q

What receptor does angiotensin 1-7 act on?

A

Mas (cardioprotective)

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6
Q

T-F there is a route from angiotensin1 to angiotensin (1-7) that does not use ACE?

A

True—endopeptidases

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7
Q

The classical ACE-AII-AT1 receptor axis is known to cause what?

A

stroke, hypertension and cardiovasc. events

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8
Q

What are the 4 mechanisms by which renin secretion is controlled?

A
  1. Renal vascular receptor- low stretch inc renin
  2. Macula densa receptor- low na inc renin
  3. SNa
    4AII, AVP, K all inhibit renin release (negative feedback)
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9
Q

What to mechanisms increase renin release in regards to lower arterial pressure?

A
  1. renal baroreceptors

2. Systemi baroreceptors through SNa

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10
Q

What are the 3 things that stimulate Renin release?

A
  1. lowered arterial pressure
  2. Dehydration, hemorrhage
  3. hyponatremia
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11
Q

What are the 4 actions that raises arterial pressure from angiotensin?

A
  1. direct vasoconstriction in smooth muscle
  2. CNS up SNa and Vasopressin release
  3. Norepinephrine release from sympathetic neurons
  4. Adrenal medulla stim release of epi
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12
Q

Can angiotensin peptides cause hypertrophy?

A

Yes, by hemodynamic and non-hemodynamic mechanisms

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13
Q

What does angiotensin stimulate in the CNS? adrenal?

A

Thirst, and ACTH from pituitary

aldosterone

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14
Q

How is R?A system detrimental to the heart? what counteracts?

A

heart failure diminishes renal flow, renin up, AII up leads to increased peripheral resistance (after load) and increased H2O (preload)—thus exacerbating the condition.

angiotensin (1-7) counteracts

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15
Q

How does angiotensin promote sodium retention? regulate its own production?

A
  1. vasoconstriction and incr. proximal tubular Na reabsorption
  2. decr. renin release neg feedback
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16
Q

What is the outcome of AT1R activation? AT2R?

A
  1. Gq–> stim phospholipase C–> up Ca, MapK- vasoconstriction
  2. Does not activate above– incr. NO and blocks MAPK- vasodilation (may be beneficial for AT1R blockers, AII effects are much stronger on AT1R vasoconstriction)
17
Q

What does the MAS receptor mediate? stimulates what?

A

vasodilation, anti-inflammatory, anti-cell prolix, stimulates up Ca and NO

18
Q

What do ARBs have higher affinity for? do the affect kininase II? blockade results in loss of what?

A
  1. AT1R»AT2R
  2. no
  3. AII feedback inhibition of renin release from kidney
19
Q

Ang(1-7) is promoted from extra angiotensin I when ACE is blocked. What other mechanisms increase Ang-(1-7) when ACE is blocked?

A

Degradation of Ang(1-7) by ACE is also impaired

20
Q

RAS blockade has little effect in normotensive patients, except for what occasion?

A

Na depleted individuals

21
Q

Where is RAS produced/used on a local bases?

A

vascular smooth muscle

Brain

22
Q

What does plasma kallikrein activate? tissue kallikrein?

A

bradykinin

kallidin

23
Q

What are kinin’s effects on arterioles [4]? When? large arteries?

A
  1. a. vasodilation via NO and eicosanoids, b. incr. capillary permeability, c. stim SNa, d. stimulate EPI
  2. in hypertensive situations, but not for maintenance
  3. constrict large arteries and veins
24
Q

Does bradykinin promote inflammation? pain? receptor?

A

yes and yes, GPCR B2 [up PLC increase Ca, up PLA2 increase eicosanoids]

25
Q

Do ACE inhibitors decrease bradykinin half life?

A

No they increase it

26
Q

When is vasopressin released?

A

low arterial P, low fluid volume or high plasma osmol, pain/nausea/hypoxia

27
Q

Physiologic actions of vasopressin?

A
  1. antidiuretic
  2. direct vasoconstriction (reflex bradycardia)
  3. indirect central actions–activate vagal–> bradycardia
28
Q

What vasopressin receptor is for antidiuretic effects? CV effects?

A
  1. V2– up cAMP

2. V1– up phospholipase C–> up Ca2